Acute Pancreatitis

Acute pancreatitis is a relatively common condition presenting with severe, acute, constant epigastric pain. Incidence of ~5 per 100,000/year. Acute pancreatitis has a significant mortality. Early complications include acute renal failure, DIC, hypocalcemia and ARDS. Treatment of pancreatitis is mainly supportive and includes “pancreatic rest”. Withholding food or liquids by mouth until symptoms subside, and adequate narcotic analgesia. At the core surgical training interview clinical station you may be asked how you would assess and manage a patient presenting with acute epigastric pain.


Pathology:                 

Inflammation of the pancreas with release of inflammatory cytokines and pancreatic enzymes. Acute pancreatitis is an acute inflammatory process caused by the effects of enzymes released from the pancreatic acini.


Differential Diagnosis

  • Peptic Ulcer disease
  • Intestinal Obstruction
  • Triple A (AAA)
  • Gall stone disease
  • Viral gastroenteritis
  • Myocardial Infarction


Aetiology:                 

‘GET SMASHED’

Gallstones

Ethanol

Trauma

Steroids

Mumps

Autoimmune

Scorpion stings

Hyperthermia, Hyperlipidaemia

ERCP

Drugs: NSAIDs, Thiazide diuretics, Azathioprine, Isoniazid


Pathogenesis

Duct obstruction: may lead to reflux of bile into the pancreatic ducts causing injury; increased intraductal pressure may damage pancreatic acini, leading to leakage of pancreatic enzymes with further damage to pancreas.

Direct acinar damage: due to viruses, bacteria, drugs or trauma. Protease release causes widespread destruction of pancreas and increases further enzyme release with consequent further damage.

Lipase causes fat necrosis, resulting in characteristic yellowish-white flecks on the pancreas, mesentery and omentum, often with calcium deposition (fat necrosis).

Elastase destroys blood vessels, leading to haemorrhage within the pancreas and haemorrhagic exudate into the peritoneum.

Haemorrhage may be extensive, leading to acute haemorrhagic pancreatitis.


Biochemical Changes

Increased serum amylase: released from damaged acini into bloodstream.

Hypocalcaemia: arises because of deposition of calcium in areas of fat necrosis.

Hyperglycaemia: occurs because of associated damage to pancreatic islets.

Abnormal liver function tests, especially raised bilirubin and alkaline phosphatase, due to mild obstruction of bile ducts by oedema.


Symptoms:                

Epigastric pain radiating to back, relieved sitting forward, 

Nausea, 

Vomiting

 

Signs:                         

Epigastric tenderness and guarding, septic shock

Cullen’s Sign: Periumbilical bruising

Grey-Turner’s Sign: Bilateral flank bruising indicates pancreatic necrosis with

retroperitoneal bleeding

 

Investigations:         

Bloods: FBC, U&E, LFTs, serum amylase >1000Iu/mL, lipase, blood gas

Imaging: Abdominal X-Ray - loss of psoas shadow indicates retroperitoneal fluid

Ultrasound Abdomen: gallstones, pancreatic fluid

CT Abdomen: pancreatic inflammation, fluid

core surgery interview pancreatitis 

Treatment:               

Medical: IV fluids, oxygen, analgesia and assess severity

If severe, transfer to HDU/ITU for monitoring of vital signs and fluid balance with nutritional support

 

Complications:         

Pancreatic pseudocyst or necrosis, 

Chronic pancreatitis, 

ARDS, 

SIRS, 

Death

 

Prognosis:                 

Several classification systems for severity Modified Glasgow, Ranson and APACHE II

Modified Glasgow Scoring For Pancreatitis: 

Mnemonic – ‘PANCREAS’

3 or more criteria in first 48 hours indicates a severe attack

PaO2 <8KPa

Age >55 years

Neutrophils >15x109/L

Calcium <2mmol/L

Renal Function Urea >16mmol/L

Enzymes LDH >600IU/L or AST >2000IU/L

Albumin <32g/L

Sugar >10mmol/L


Mortality

Overall mortality is 10–20%

Severe haemorrhagic pancreatitis has mortality rate of 50%. 

The Usual cause of mortality is multiple organ failure.